The migration of retinal glial cells to extra-retinal sites is an important aspect of the pathophysiology of many proliferative retinopathies including proliferative vitreoretinopathy (PVR), and fibovascular-retinopathies such as diabetic vitreoretinopathy, retinopathy of prematurity, and traumatic vitreoretinopathy. The most attractive hypothesis which accounts for gliosis as a final common pathway in these pathologies is the secretion or release of a protein by the retina which stimulates the migration and growth of retinal glia under a variety of physiological and pathological stresses. We have purified a protein from normal bovine retina which elicites a migratory response in various neural glia, which we have named the retinal chemotactic protein. The research proposed here will provide an accurate determination of the physical properties of the retinal chemotactic protein and measure its effect on the migration, proliferation, and deposition of extracellular matrix by retinal glia in vitro. Studies of ocular cells in vitro will determine the physiological parameters regulating the release or secretion of this protein. This work will further establish the role of the retinal chemotactic protein in retinal detachment using the cat animal model. Finally, vitreous aspirates and celullar membranes removed during vitrectomy will be used to establish the role of this same protein in human pathologies involving glial migration and proliferation. This work will provide a basic understanding of the retina's response to injury. Since proliferated glial cells directly interfere with retinal reattachment, and may provide a structure upon which other ocular cell types may attach and divide, these results should lead to an enhanced ability to design new forms of treatment for these devastating retinal diseases.